Component

Insulin receptor / INSR

Independent biological entity. Read linked claims for experimental scope and context.

6 recorded relationships. Experimental role, claim status and evidence remain attached to each record.

Read recorded mechanisms Open recursive mind map

How nutrients influence it

Every nutrient with a recorded effect on this component, credited to the nutrient that acted rather than the chapter that recorded it. Open a nutrient to see the findings and the conditions they were measured under.

How nutrients reach it in more than one step

Chains of two or more recorded steps that end here, grouped by the nutrient they start from. Each step is a separate finding, so a chain is a route a mechanism could take, not proof that it does.

Tracing routes…

What it does

Every recorded relationship this component is part of, grouped by its role. Plain wording comes first; the technical statement follows.

Recorded relationships

What it acts on

  1. INSR silencing diminished the insulin-dependent increase in glucose consumption associated with berberine-enhanced receptor expression.

    Insulin receptor / INSR → Cellular glucose consumption source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    machinery_impairment Imported condition classification; unverified.
    evidence_span
    {"source_cache": "artifacts/berberine-research/19059538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23", "start_char": 0, "end_char": 1461, "text_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23"}
    experimental_model
    Promoter assays, gene silencing and insulin-dependence experiments
    exposure
    Berberine with or without insulin, INSR siRNA or PKC inhibition
    limitations
    This insulin-dependent route does not replace insulin in insulin-deficient disease. Other models show insulin-independent routes; those observations are not discarded.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Human liver cells and separate rodent experiments
    plain_language
    A sensitizing signal cannot substitute for missing receptor machinery.
    primary_references
    [berberine-p19059538] Berberine reduces insulin resistance through protein kinase C-dependent up-regulation of insulin receptor expression. (2009). https://pubmed.ncbi.nlm.nih.gov/19059538/ DOI: 10.1016/j.metabol.2008.08.013
    tissue_or_cell_type
    Insulin receptor expression and glucose consumption
    trigger_kind
    machinery_impairment Imported condition classification; unverified.

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 506–517

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Promoter assays, gene silencing and insulin-dependence experiments · source_derived_draft · unverified_draft

    ### berberine-insr-loss INSR silencing diminished the insulin-dependent increase in glucose consumption associated with berberine-enhanced receptor expression. Condition category: machinery_impairment nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: A sensitizing signal cannot substitute for missing receptor machinery. organism: Human liver cells and separate rodent experiments tissue_or_cell_type: Insulin receptor expression and glucose consumption experimental_model: Promoter assays, gene silencing and insulin-dependence experiments limitations: This insulin-dependent route does not replace insulin in insulin-deficient disease. Other models show insulin-independent routes; those observations are not discarded. exposure: Berberine with or without insulin, INSR siRNA or PKC inhibition evidence_span: {"source_cache": "artifacts/berberine-research/19059538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23", "start_char": 0, "end_char": 1461, "text_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23"} [berberine-p19059538] Berberine reduces insulin resistance through protein kinase C-dependent up-regulation of insulin receptor expression. (2009). https://pubmed.ncbi.nlm.nih.gov/19059538/ DOI: 10.1016/j.metabol.2008.08.013
    Complete structured claim and evidence

What acts on it

  1. After vanadyl treatment, muscle showed trends toward increased basal insulin-receptor, IRS1 and Shc tyrosine phosphorylation and IRS1-associated PI3K activity without additional insulin-stimulated increases.

    Vanadyl sulfate → Insulin receptor / INSR source_derived_draftungraded
    Experimental context and source evidence
    evidence_access
    Primary abstract
    experimental_model
    Human muscle samples from the same 16-person trial.
    limitations
    Reported as trends; phosphorylation patterns did not clearly correlate with glucose disposal. No proven nutrient requirement.
    nutrient_topic
    Vanadium collection; molecular form, preparation, species, exposure and manipulation remain explicit. · Vanadium
    plain_language
    Early signaling markers did not guarantee a larger response to insulin.
    primary_references
    Metabolic effects of vanadyl sulfate in humans with non-insulin-dependent diabetes mellitus: in vivo and in vitro studies. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10726921/ · DOI 10.1016/s0026-0495(00)90418-9

    Vanadium: speciation, phosphate-sensitive enzymes and cross-nutrient mechanisms (2026-09-19) · lines 390–396

    AI-assisted research curation; primary references, access levels and experimental limitations individually identified. Not publisher full text. · supports · Human muscle samples from the same 16-person trial. · source_derived_draft · unverified_draft

    ## vanadium-human-signaling Early signaling markers did not guarantee a larger response to insulin. After vanadyl treatment, muscle showed trends toward increased basal insulin-receptor, IRS1 and Shc tyrosine phosphorylation and IRS1-associated PI3K activity without additional insulin-stimulated increases. Model: Human muscle samples from the same 16-person trial. Limitations: Reported as trends; phosphorylation patterns did not clearly correlate with glucose disposal. No proven nutrient requirement. Evidence access: Primary abstract Metabolic effects of vanadyl sulfate in humans with non-insulin-dependent diabetes mellitus: in vivo and in vitro studies. · 2000 · https://pubmed.ncbi.nlm.nih.gov/10726921/ · DOI 10.1016/s0026-0495(00)90418-9
    Complete structured claim and evidence

  2. Berberine increased INSR mRNA and protein in human liver cells through PKC-dependent promoter activation.

    Berberine → Insulin receptor / INSR source_derived_draftungraded
    Experimental context and source evidence
    evidence_span
    {"source_cache": "artifacts/berberine-research/19059538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23", "start_char": 0, "end_char": 1461, "text_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23"}
    experimental_model
    Promoter assays, gene silencing and insulin-dependence experiments
    exposure
    Berberine with or without insulin, INSR siRNA or PKC inhibition
    limitations
    This insulin-dependent route does not replace insulin in insulin-deficient disease. Other models show insulin-independent routes; those observations are not discarded.
    nutrient_topic
    Berberine research collection; topical membership is not evidence of a direct dietary effect. · Berberine
    organism
    Human liver cells and separate rodent experiments
    plain_language
    The cells increased the machinery that receives an insulin signal.
    primary_references
    [berberine-p19059538] Berberine reduces insulin resistance through protein kinase C-dependent up-regulation of insulin receptor expression. (2009). https://pubmed.ncbi.nlm.nih.gov/19059538/ DOI: 10.1016/j.metabol.2008.08.013
    tissue_or_cell_type
    Insulin receptor expression and glucose consumption

    Berberine: metabolism, nutrient connections and drug interactions (2026-09-17) · lines 493–504

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Promoter assays, gene silencing and insulin-dependence experiments · source_derived_draft · unverified_draft

    ### berberine-insr-expression Berberine increased INSR mRNA and protein in human liver cells through PKC-dependent promoter activation. Condition category: normal nutrient_topic: Berberine research collection; topical membership is not evidence of a direct dietary effect. plain_language: The cells increased the machinery that receives an insulin signal. organism: Human liver cells and separate rodent experiments tissue_or_cell_type: Insulin receptor expression and glucose consumption experimental_model: Promoter assays, gene silencing and insulin-dependence experiments limitations: This insulin-dependent route does not replace insulin in insulin-deficient disease. Other models show insulin-independent routes; those observations are not discarded. exposure: Berberine with or without insulin, INSR siRNA or PKC inhibition evidence_span: {"source_cache": "artifacts/berberine-research/19059538.abstract.txt", "locator": "Primary indexed abstract; zero-based, end-exclusive Unicode character offsets", "file_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23", "start_char": 0, "end_char": 1461, "text_sha256": "70e22b36b13efcbb36d7f27b417fe72dc96ba2f384f01a8d037bfc2d3213ef23"} [berberine-p19059538] Berberine reduces insulin resistance through protein kinase C-dependent up-regulation of insulin receptor expression. (2009). https://pubmed.ncbi.nlm.nih.gov/19059538/ DOI: 10.1016/j.metabol.2008.08.013
    Complete structured claim and evidence

Where it participates (unsigned role)

  1. Insulin receptor autophosphorylation was reduced about 50% in muscle preparations from Mg-deficient rats, despite similar insulin binding.

    Magnesium → Insulin receptor autophosphorylation source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Magnesium -> insulin signaling -> carbohydrate handling.
    experimental_model
    Partially purified rat gastrocnemius receptors.
    limitations
    A depletion experiment; not isolated Mg binding to a particular receptor site.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Rattus norvegicus
    plain_language
    The receptor could still bind insulin, but its downstream activation was impaired.
    primary_references
    [mg-suarez1995] Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats (1995). https://pubmed.ncbi.nlm.nih.gov/8582534/ DOI: 10.1007/bf00401757
    tissue_or_cell_type
    Rat gastrocnemius receptor preparations and perfused hindquarter
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1503–1513

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Partially purified rat gastrocnemius receptors. · source_derived_draft · unverified_draft

    ### mg-deficiency-insr-autophosphorylation Insulin receptor autophosphorylation was reduced about 50% in muscle preparations from Mg-deficient rats, despite similar insulin binding. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The receptor could still bind insulin, but its downstream activation was impaired. organism: Rattus norvegicus tissue_or_cell_type: Rat gastrocnemius receptor preparations and perfused hindquarter experimental_model: Partially purified rat gastrocnemius receptors. limitations: A depletion experiment; not isolated Mg binding to a particular receptor site. cross_nutrient: Magnesium -> insulin signaling -> carbohydrate handling. [mg-suarez1995] Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats (1995). https://pubmed.ncbi.nlm.nih.gov/8582534/ DOI: 10.1007/bf00401757
    Complete structured claim and evidence

  2. Mg-deficient rat muscle had lower glucose uptake at submaximal insulin; basal and maximal-insulin uptake were preserved.

    Magnesium → Insulin-stimulated glucose uptake source_derived_draftungraded
    Experimental context and source evidence
    availability_state
    nutrient_deficiency Imported condition classification; unverified.
    cross_nutrient
    Magnesium/insulin/glucose; impaired sensitivity is distinct from absence of transport.
    experimental_model
    Perfused rat hindquarter.
    limitations
    Muscle GLUT4 abundance was similar; the experiment does not establish a single causal intermediate.
    nutrient_topic
    Magnesium research collection; topical membership is not evidence of a direct dietary effect. · Magnesium
    organism
    Rattus norvegicus
    plain_language
    The response became less sensitive rather than completely stopping.
    primary_references
    [mg-suarez1995] Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats (1995). https://pubmed.ncbi.nlm.nih.gov/8582534/ DOI: 10.1007/bf00401757
    tissue_or_cell_type
    Rat gastrocnemius receptor preparations and perfused hindquarter
    trigger_kind
    nutrient_deficiency Imported condition classification; unverified.

    Magnesium: cross-nutrient mechanisms and deficiency (2026-09-17) · lines 1515–1525

    AI-assisted literature curation; primary study URLs and scope retained in the document and extraction. Not publisher full text. · supports · Perfused rat hindquarter. · source_derived_draft · unverified_draft

    ### mg-deficiency-muscle-insulin-response Mg-deficient rat muscle had lower glucose uptake at submaximal insulin; basal and maximal-insulin uptake were preserved. Condition category: nutrient_deficiency nutrient_topic: Magnesium research collection; topical membership is not evidence of a direct dietary effect. plain_language: The response became less sensitive rather than completely stopping. organism: Rattus norvegicus tissue_or_cell_type: Rat gastrocnemius receptor preparations and perfused hindquarter experimental_model: Perfused rat hindquarter. limitations: Muscle GLUT4 abundance was similar; the experiment does not establish a single causal intermediate. cross_nutrient: Magnesium/insulin/glucose; impaired sensitivity is distinct from absence of transport. [mg-suarez1995] Impaired tyrosine-kinase activity of muscle insulin receptors from hypomagnesaemic rats (1995). https://pubmed.ncbi.nlm.nih.gov/8582534/ DOI: 10.1007/bf00401757
    Complete structured claim and evidence

  3. Phlorizin and vanadate both prevented diabetes-associated hepatic insulin-receptor overexpression in vivo, but only vanadate directly lowered transcripts in hepatoma cells.

    Phlorizin → Liver insulin-receptor expression in streptozotocin-diabetic rats source_derived_draftungraded
    Experimental context and source evidence
    dose
    Daily phlorizin or vanadate from days 5-23; direct cell exposures
    duration
    18 days in rats; 4 hours in cells
    evidence_access
    Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    evidence_scope
    literature_reviewed; model-specific source-derived curation
    experimental_model
    Streptozotocin-diabetic rats and Fao hepatoma cells
    limitations
    The contrast supports an indirect glycemia route for phlorizin and a distinct direct action for vanadate.
    nutrient_topic
    Phlorizin chapter; interacting nutrients, drugs, peptides and proteins retain their experimental settings. · Phlorizin
    organism
    Streptozotocin-diabetic rats and Fao hepatoma cells
    plain_language
    Phlorizin and vanadate both prevented diabetes-associated hepatic insulin-receptor overexpression in vivo, but only vanadate directly lowered transcripts in hepatoma cells.
    primary_references
    Treatment of streptozotocin-induced diabetic rats with vanadate and phlorizin prevents the over-expression of the liver insulin receptor gene. (1999). https://pubmed.ncbi.nlm.nih.gov/10037256/ DOI: 10.1530/eje.0.1400079
    route
    In vivo and in vitro
    tissue
    Insulin-receptor number and mRNA

    Phlorizin: mechanism of action and interactions (2026-09-20) · lines 132–141

    Original AI-assisted source-specific curation with primary-study citations, model, exposure, route, duration, negative findings and limitations preserved. Not publisher full text. · supports · Streptozotocin-diabetic rats and Fao hepatoma cells · source_derived_draft · unverified_draft

    ## phlorizin-vanadate-comparator Phlorizin and vanadate both prevented diabetes-associated hepatic insulin-receptor overexpression in vivo, but only vanadate directly lowered transcripts in hepatoma cells. Model/species: Streptozotocin-diabetic rats and Fao hepatoma cells Tissue/system: Insulin-receptor number and mRNA Exposure: Daily phlorizin or vanadate from days 5-23; direct cell exposures Route: In vivo and in vitro Duration: 18 days in rats; 4 hours in cells Limits: The contrast supports an indirect glycemia route for phlorizin and a distinct direct action for vanadate. Primary reference: Treatment of streptozotocin-induced diabetic rats with vanadate and phlorizin prevents the over-expression of the liver insulin receptor gene. (1999). https://pubmed.ncbi.nlm.nih.gov/10037256/ DOI: 10.1530/eje.0.1400079 Access: Primary PubMed abstract and indexed metadata reviewed. Full-text method details not stated here remain unresolved.
    Complete structured claim and evidence

In the sources

Preserved passages that mention this component, quoted exactly. Open one to read it in context.

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